PTSD Increases Risk for Hypertension Development Through PVN Activation and Vascular Dysfunction in Sprague Dawley Rats DOI Creative Commons
Xinqian Chen, Xin Yan, Chunxiu Yu

et al.

Antioxidants, Journal Year: 2024, Volume and Issue: 13(11), P. 1423 - 1423

Published: Nov. 20, 2024

This study investigates the impact of single prolonged stress (SPS), a model post-traumatic disorder (PTSD), on cardiovascular responses, hypothalamic paraventricular nucleus (PVN) activity, and vascular function to elucidate mechanisms linking traumatic hypertension. Although SPS did not directly cause chronic hypertension in male Sprague Dawley (SD) rats, it induced acute but transient increases blood pressure heart rate significantly altered expression hypertension-associated genes, such as vasopressin, angiotensin II type 1 receptor (AT1R), FOSL1 PVN. Notably, mitochondrial reactive oxygen species (mtROS) were predominantly elevated pre-autonomic regions PVN, colocalizing with AT1R- FOSL1-expressing cells, suggesting that oxidative may amplify sympathetic activation responses. also increased mRNA levels pro-inflammatory cytokines (TNFα IL1β) inducible nitric oxide synthase (iNOS) aorta, impaired reactivity vasoconstrictor vasodilator stimuli, reflecting compromised function. These findings suggest SPS-sensitize neuroendocrine, autonomic, pathways create state vulnerability could predispose individuals when exposed additional stressors. Understanding these provides critical insights into pathophysiology stress-related disorders underscores need for targeted therapeutic interventions address modulate PVN mitigate PTSD related conditions.

Language: Английский

Placental ischemia during pregnancy induces hypertension, cerebral inflammation, and oxidative stress in dams postpartum DOI Creative Commons

Savanna Smith,

Jonna Smith,

Kylie Jones

et al.

Hypertension in Pregnancy, Journal Year: 2025, Volume and Issue: 44(1)

Published: Jan. 30, 2025

Preeclampsia (PE) is characterized as de novo hypertension (HTN) with end-organ damage, especially in the brain. PE hypothesized to be caused by placental ischemia. affects ~5-8% of USA pregnancies and increases risk for HTN cerebrovascular diseases (CVD) later life. We hypothesize that blood pressure (BP), cerebral oxidative stress, inflammation will increase postpartum (PP) ischemic dams. Placental ischemia was induced pregnant Sprague Dawley dams, utilizing reduced uterine perfusion (RUPP) surgery. At 6 weeks PP (~3 human years), BP measured via carotid catheterization, stress were assessed ELISAs, biochemical assays, Western blots. BP, pro-inflammatory cytokines (TNF-α IL-6), GFAP (a marker astrocyte activity) increased RUPP Cerebral hydrogen peroxide (H2O2) also had a strong correlation proinflammatory (TNF- α activation. dams have at postpartum. These changes may contribute pathology development CVDs

Language: Английский

Citations

0
cFos-mediated β-Arrestin1 in the RVLM alleviates sympathetic hyperactivity induced by ovariectomy DOI

Jiuqiong Yan,

Meng Qi,

Hao Fan

et al.

Molecular and Cellular Endocrinology, Journal Year: 2025, Volume and Issue: unknown, P. 112520 - 112520

Published: March 1, 2025

Language: Английский

Citations

0
Hypothalamic Gliosis Is Associated With Multiple Cardiovascular Disease Risk Factors in the Framingham Heart Study DOI Creative Commons
Justin Lo, Susan J. Melhorn,

Sarah Kee

et al.

Journal of the American Heart Association, Journal Year: 2025, Volume and Issue: unknown

Published: April 16, 2025

Background Hypothalamic gliosis is mechanistically linked to obesity and insulin resistance in rodent models. We tested cross‐sectional associations between radiologic measures of hypothalamic humans clinically relevant cardiovascular disease risk factors, as well prevalent coronary heart disease. Methods Results Using brain magnetic resonance imaging from FHS (Framingham Heart Study) participants (N=867; mean age, 55 years; 55% women), T2‐signal intensities were extracted bilaterally the region interest mediobasal hypothalamus (MBH) reference regions amygdala putamen. ratios created which greater relative intensity suggests gliosis. The primary measure compared MBH with (MBH/amygdala). Outcomes body mass index, high‐density lipoprotein cholesterol, low‐density fasting triglycerides, presence hypertension (n=449), diabetes (n=66), metabolic syndrome (n=254), or (n=25). Statistical testing was performed using linear logistic regression. Greater MBH/amygdala associated higher index ( P <0.001), triglycerides lower cholesterol =0.034), =0.0088), latter 2 independent index. Findings for mixed, whereas strongly <0.001). not (all >0.05), but CIs wide. Conclusions a well‐established study development, we found evidence linking multiple adiposity. Our results highlight need consider central nervous system mechanisms understand improve cardiometabolic health.

Language: Английский

Citations

0
Hypothalamic Gliosis is Associated with Multiple Cardiovascular Disease Risk Factors DOI Creative Commons
Justin Lo, Susan J. Melhorn,

Sarah Kee

et al.

medRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: Sept. 22, 2024

Abstract Background Hypothalamic gliosis is mechanistically linked to obesity and insulin resistance in rodent models. We tested cross-sectional associations between radiologic measures of hypothalamic humans clinically relevant cardiovascular disease risk factors, as well prevalent coronary heart disease. Methods Using brain MRI images from Framingham Heart Study participants (N=867; mean age, 55 years; 55% females), T2 signal intensities were extracted bilaterally the region interest mediobasal hypothalamus (MBH) reference regions amygdala (AMY) putamen (PUT). ratios created which greater relative intensity suggests gliosis. The primary measure compared MBH AMY (MBH/AMY); a positive control ratio (MBH/PUT) also assessed whereas negative (PUT/AMY) did not. Outcomes BMI, HDL-C, LDL-C, fasting triglycerides, presence hypertension (n=449), diabetes mellitus (n=66), metabolic syndrome (n=254), or (n=25). Dietary factors for prospective analysis. Statistical testing was performed using linear logistic regression. Results Greater MBH/AMY associated with higher BMI (β = 21.5 [95% CI, 15.4– 27.6]; P <0.001), triglycerides 1.1 0.6–1.7]; lower HDL-C –20.8 –40.0 –1.6]; =0.034), (odds ratio, 1.2 1.1–1.4]; =0.0088), latter two independent BMI. Findings mixed attenuated by adjusting Metabolic 1.3 1.1–1.6]; <0.001). Model results almost uniformly confirmed ratios, that not test unrelated any outcomes (all ≥0.05). >0.05), but confidence intervals wide. Self-reported percentages macronutrient intake consistently related future ratios. Conclusions well-established study development, we found evidence linking multiple even adiposity. Our highlight need consider neurologic mechanisms understand improve cardiometabolic health.

Language: Английский

Citations

1
The brain and hypertension: how the brain regulates and suffers from blood pressure DOI
Keisuke Shinohara

Hypertension Research, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 14, 2024

Language: Английский

Citations

0
PTSD Increases Risk for Hypertension Development Through PVN Activation and Vascular Dysfunction in Sprague Dawley Rats DOI Creative Commons
Xinqian Chen, Xin Yan, Chunxiu Yu

et al.

Antioxidants, Journal Year: 2024, Volume and Issue: 13(11), P. 1423 - 1423

Published: Nov. 20, 2024

This study investigates the impact of single prolonged stress (SPS), a model post-traumatic disorder (PTSD), on cardiovascular responses, hypothalamic paraventricular nucleus (PVN) activity, and vascular function to elucidate mechanisms linking traumatic hypertension. Although SPS did not directly cause chronic hypertension in male Sprague Dawley (SD) rats, it induced acute but transient increases blood pressure heart rate significantly altered expression hypertension-associated genes, such as vasopressin, angiotensin II type 1 receptor (AT1R), FOSL1 PVN. Notably, mitochondrial reactive oxygen species (mtROS) were predominantly elevated pre-autonomic regions PVN, colocalizing with AT1R- FOSL1-expressing cells, suggesting that oxidative may amplify sympathetic activation responses. also increased mRNA levels pro-inflammatory cytokines (TNFα IL1β) inducible nitric oxide synthase (iNOS) aorta, impaired reactivity vasoconstrictor vasodilator stimuli, reflecting compromised function. These findings suggest SPS-sensitize neuroendocrine, autonomic, pathways create state vulnerability could predispose individuals when exposed additional stressors. Understanding these provides critical insights into pathophysiology stress-related disorders underscores need for targeted therapeutic interventions address modulate PVN mitigate PTSD related conditions.

Language: Английский

Citations

0